Greater reduction is labeled dihydroalprenolol binding to lymphocyte membrane protein occurred in asthmatic patients. This observation suggests that Beta-adrenergic receptor abnormalities may play a role in the pathogenesis and severity of bronchial asthma. In addition, individuals with the most severe disease showed evidence of more hyperresponsive airway to the inhalation of methacholine aerosol. The exact relationship between Beta-adrenergic receptor defects and airway hyperreactivity needs further study. Platelet aggregation abnormalities were associated with high IgE antibody levels and less clinically severe asthma. Occupational asthma due to toluene diisocyanate (TDI) seems to provide a good model for studying beta receptor function since in vitro studies with TDI results in decrease Beta-adrenergic function. This investigation emphasizes the importance of nonimmunological mechanisms in influencingdisease severity in bronchial asthma. It is the overall goal of this study that this information might better elucidate nonimmunologic mechanisms in asthma in hopes of providing a more rational approach to treatment.